ReviewFrontiers in immunology2026
Immune-metabolic convergence in skeletal remodeling disorders: shared osteoimmune, senescent and lipid mechanisms across aging-related and immune-mediated bone disease.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Bone and joint disorders of the aging musculoskeletal system are conventionally treated as separate clinical entities. This disease-centered view aids diagnosis but obscures the immune, inflammatory, senescent and metabolic programs they share. This Review compares five of them, grouped by etiology rather than by age: two aging-driven remodeling disorders, osteoporosis (OP) and osteoarthritis (OA); two immune-mediated arthritides in which aging modifies rather than causes the skeletal outcome, rheumatoid arthritis (RA) and psoriatic arthritis (PsA); and one focal, largely monogenic disorder included as a boundary case, Paget's disease of bone (PDB). RA and PsA are not treated as age-related diseases; they are included because they show most directly that immune activation alone can redirect skeletal remodeling. The review is narrative and mechanism-oriented, based on a structured, auditable search (Section 2); we compare evidence across diseases rather than claim exhaustive synthesis. Skeletal aging, immunosenescence, inflammaging and lipid dysregulation converge on five nodes: the receptor activator of nuclear factor-κB ligand (RANKL)-osteoprotegerin (OPG) axis, the interleukin-17/tumor necrosis factor-α/interleukin-6 network, senescence-associated secretory phenotype (SASP) amplification, phospholipid peroxidation and ferroptosis, and Wnt-sclerostin-Dickkopf-1 (DKK-1) balance. Across diseases these nodes generate different skeletal outputs: systemic bone loss in OP; cartilage degeneration with subchondral remodeling in OA; erosion with impaired repair in RA; erosion combined with ectopic bone formation in PsA; and focal high-turnover remodeling in PDB. Disease identity, we argue, is set by the sign and relative weighting of node activity rather than by which nodes are engaged; the opposing direction of DKK-1 regulation in RA and PsA is the clearest example. Ferroptotic injury is resolved by cell type rather than treated as uniformly harmful, and PDB is retained as a comparator showing that shared-node activation is permissive rather than deterministic. Candidate biomarkers and pathway-directed therapies are summarized with their translational gaps. Every disease × mechanism combination is graded on a four-level evidence scheme (E1, established human evidence, to E4, indirect or
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